Acute Toxicity of Jinchuan Formula Plum Wine Extract and Its Protective Effect on Mice with Liver Injury

[Objectives]To investigate the acute toxicity and hepatoprotective effect of Jinchuan formula plum wine extract on mice,determine its safety range,and evaluate its hepatoprotective effect.[Methods]The median lethal dose(LD_(50))was determined by acute toxicity test with the toxic reaction and mortality of mice as indexes.Sixty Kunming mice were randomly divided into 6 groups:normal control group,model group(ConA-induced liver injury model),Jinchuan formula plum wine high,medium and low dose groups(1.0,0.5,0.25 g/kg)and silybin group(0.1 g/kg).The levels of ALT,AST,LDH in serum and TG,VLDL in liver were measured.After HE staining,the pathological changes of liver tissue in mice were observed,and the liver protective effect of Jinchuan formula plum wine extract was analyzed and evaluated.[Results]LD_(50)was 11.18 g/kg,and the 95%confidence limit of LD_(50)was 10.31-12.05 g/kg.The high-dose group of Jinchuan formula plum wine extract could significantly reduce the serum ALT and AST activities of ConA-induced liver injury mice(P<0.05).[Conclusions]Jinchuan formula plum wine extract is relatively safe,and also has a protective effect on liver injury.

Novel miR-490-3p/hnRNPA1-b/PKM2 axis mediates the Warburg effect and proliferation of colon cancer cells via the PI3K/AKT pathway

BACKGROUND Heterogeneous ribonucleoprotein A1(hnRNPA1)has been reported to enhance the Warburg effect and promote colon cancer(CC)cell proliferation,but the role and mechanism of the miR-490-3p/hnRNPA1-b/PKM2 axis in CC have not yet been elucidated.AIM To investigate the role and mechanism of a novel miR-490-3p/hnRNPA1-b/PKM2 axis in enhancing the Warburg effect and promoting CC cell proliferation through the PI3K/AKT pathway.METHODS Paraffin-embedded pathological sections from 220 CC patients were collected and subjected to immunohistochemical analysis to determine the expression of hnRNPA1-b.The relationship between the expression values and the clinicopathological features of the patients was investigated.Differences in mRNA expression were analyzed using quantitative real-time polymerase chain reaction,while differences in protein expression were analyzed using western blot.Cell proliferation was evaluated using the cell counting kit-8 and 5-ethynyl-2’-deoxyuridine assays,and cell cycle and apoptosis were detected using flow cytometric assays.The targeted binding of miR-490-3p to hnRNPA1-b was validated using a dual luciferase reporter assay.The Warburg effect was evaluated by glucose uptake and lactic acid production assays.RESULTS The expression of hnRNPA1-b was significantly increased in CC tissues and cells compared to normal controls(P<0.05).Immunohistochemical results demonstrated significant variations in the expression of the hnRNPA1-b antigen in different stages of CC,including stage I,II-III,and IV.Furthermore,the clinicopathologic characterization revealed a significant correlation between hnRNPA1-b expression and clinical stage as well as T classification.HnRNPA1-b was found to enhance the Warburg effect through the PI3K/AKT pathway,thereby promoting proliferation of HCT116 and SW620 cells.However,the proliferation of HCT116 and SW620 cells was inhibited when miR-490-3p targeted and bound to hnRNPA1-b,effectively blocking the Warburg effect.CONCLUSION These findings suggest that the novel miR-490-3p/hnRNPA1-b/PKM2 axis could provide a new strategy for the diagnosis and treatment of CC.

Preliminary study on the protective effect of electroacupuncture Neiguan acupoint pretreatment on rats with myocardial ischemia-reperfusion injury:role of the miR-214-3p/NCX1 axis

Background:Ischemia-reperfusion can worsen myocardial damage and increase the risk of death.Studies have revealed that ischemic preconditioning provides the best endogenous protection against myocardial ischemia-reperfusion injury(MIRI),and the principle of electroacupuncture(EA)preconditioning is comparable to that of myocardial ischemic preconditioning adaption.Our earlier research demonstrated that EA pretreatment inhibits the expression of calmodulin-dependent protein kinase IIδ(CaMKIIδ),sodium/calcium exchanger 1(NCX1),and cyclophilin D,hence providing protection against MIRI.However,the exact mechanism is still unknown.The expression of NCX1 mRNA is directly regulated by microRNA-214(miR-214).Moreover,it suppresses the levels of CaMKIIδand cyclophilin D.Whether these variables contribute to EA preconditioning to improve MIRI needs to be investigated,though.This study aimed to preliminarily determine whether EA pretreatment ameliorates MIRI by modulating the miR-214-3p/NCX1 axis.Methods:We used a rat MIRI model to investigate the effect of EA pretreatment on MIRI and the expression of miR-214-3p.In addition,adenovirus injection inhibited miR-214-3p expression in the rat MIRI model,and the influence of EA pretreatment towards MIRI was observed in the context of blocked miR-214-3p expression.Both the myocardial histological abnormalities and the alterations in the ST segment of the rat electrocardiogram were analyzed.NCX1 mRNA,cyclophilin D,and CaMKIIδexpression levels were also analyzed.Results:EA pretreatment improved MIRI.In rats with MIRI,EA administration increased miR-214-3p expression while decreasing NCX1 mRNA,cyclophilin D,and CaMKIIδproteins in cardiac tissues.The beneficial effect of EA pretreatment against MIRI was reversed,coupled with elevated levels of NCX1 mRNA,cyclophilin D,and CaMKIIδprotein expression,when an adenovirus injection disrupted the expression of miR-214-3p.Conclusions:Our findings preliminarily show that EA pretreatment inhibits the expression of NCX1 mRNA,cyclophilin D,and CaMKIIδproteins via miR-214-3p,hence exerting MIRI protection.

悬移质泥沙-微囊藻毒素复合体对大型溞的毒性效应

为探究悬移质泥沙(SPM)吸附微囊藻毒素(MCs)后形成的复合体对大型溞生理特性的影响,选择MCs的典型异构体MC-LR,通过吸附动力学实验制备了不同MC-LR吸附量的SPM-MC-LR复合体,研究了复合体对大型溞(Daphnia magna)的急性毒性作用.结果表明,SPM对MC-LR的吸附过程符合拟二级动力学模型和Freundlich等温模型,拟合最大吸附量为1720μg/g,是一种以化学吸附为主导的多分子层吸附且较容易发生.SPM-MC-LR复合体对大型溞的固定率和抗氧化酶活性呈正向剂量和时间依赖,大型溞固定率最高可达93.77%;但当复合体浓度较高时(MC-LR剂量为73.52,94.53μg/g),在大型溞体内引起的氧化应激程度过高会抑制抗氧化酶活性(SOD和CAT活性较24h分别降低了21.44%、26.51%和6.2%、18.27%).相比于游离的MC-LR,SPM的存在可能增强了MC-LR对大型溞的毒性作用.

蚯蚓对2,4-DCP污染土壤的毒性响应及微生物群落影响

2.4-二氯苯酚(2.4-DCP)作为合成农药、医药的中间体,在我国广泛生产和使用,其生态危害性已引起广泛关注.然而,关于土壤动物、微生物对2.4-DCP的毒性响应知之尚少.基于此,本研究以赤子爱胜蚓(Eisenia fetida)为受试生物,从致死浓度、抗氧化系统、病理学和行为特征角度评价2.4-DCP对蚯蚓的毒性,通过高通量测序分析土壤微生物群落变化.此外,还探讨了蚯蚓对土壤中2.4-DCP的降解动力学和微生物多样性影响.结果表明,2.4-DCP对蚯蚓7 d半致死浓度(LC_(50))值为29.55 mg·kg^(-1),14 d为28.76 mg·kg^(-1);蚯蚓体内超氧化物歧化酶(SOD)随暴露时间、浓度增加总体呈下降趋势(P<0.01),而过氧化氢酶(CAT)和丙二醛(MDA)呈缓慢上升趋势(P<0.01);当2.4-DCP暴露浓度为15 mg·kg^(-1)时,14 d可使蚯蚓表皮细胞发生凹陷并破裂,浓度达到25 mg·kg^(-1)时,蚯蚓表皮细胞丧失规则细胞排列结构,肠上皮细胞发生细胞间隙扩大和破裂现象;2.4-DCP浓度越高,对蚯蚓的行为特征影响越明显;2.4-DCP在添加蚯蚓和未添加蚯蚓土壤中的降解动力学均符合一级动力学模型,在添加蚯蚓土壤中的降解速率(0.20 d^(-1))明显高于未添加(0.08 d^(-1));2.4-DCP可抑制土壤微生物群落多样性,但蚯蚓活动、蚓粪的产生可分别增加土壤中一些具有降解有机物功能的好氧、厌氧菌属丰度.本研究旨在揭示2.4-DCP与土壤动物及微生物的相互作用关系,为综合评价2.4-DCP的毒性和风险提供理论参考.

微纳米塑料在土壤-植物系统中的迁移机制及毒性效应研究进展

微塑料是指粒径小于5 mm的塑料碎屑和颗粒,其中粒径小于100 nm为纳米塑料。微纳米塑料作为一种新型污染物,具有难以降解、容易发生积累和可长距离迁移等特点,进而对生态环境产生影响。但是,与其他环境中的微纳米塑料相比,人们对土壤环境中的微纳米塑料的认识与了解还比较少。所以,本文详细阐明了微纳米塑料在土壤环境中的生物和非生物迁移过程与机制,系统总结了微纳米塑料从土壤到植物的转运过程,并探讨了微纳米塑料对植物种子萌发和根系发育产生的直接毒性效应,通过改变土壤理化性质和吸附重金属、有机污染物进而成为污染物传输载体而对植物产生的间接毒性作用。最后,提出了土壤-植物系统中微纳米塑料污染目前还需要进一步研究和处理的问题。本文可为土壤-植物系统中微纳米塑料污染的生态风险评估提供科学参考。

Neuroprotective effects of exogenous brain-derived neurotrophic factor on amyloid-beta 1-40-induced retinal degeneration

Amyloid-beta(Aβ)-related alterations,similar to those found in the brains of patients with Alzheimer's disease,have been observed in the retina of patients with glaucoma.Decreased levels of brain-derived neurotrophic factor(BDNF)are believed to be associated with the neurotoxic effects of Aβpeptide.To investigate the mechanism underlying the neuroprotective effects of BDNF on Aβ_(1-40)-induced retinal injury in Sprague-Dawley rats,we treated rats by intravitreal administration of phosphate-buffered saline(control),Aβ_(1-40)(5 nM),or Aβ_(1-40)(5 nM)combined with BDNF(1μg/mL).We found that intravitreal administration of Aβ_(1-40)induced retinal ganglion cell apoptosis.Fluoro-Gold staining showed a significantly lower number of retinal ganglion cells in the Aβ_(1-40)group than in the control and BDNF groups.In the Aβ_(1-40)group,low number of RGCs was associated with increased caspase-3 expression and reduced TrkB and ERK1/2 expression.BDNF abolished Aβ_(1-40)-induced increase in the expression of caspase-3 at the gene and protein levels in the retina and upregulated TrkB and ERK1/2 expression.These findings suggest that treatment with BDNF prevents RGC apoptosis induced by Aβ_(1-40)by activating the BDNF-TrkB signaling pathway in rats.

T-2毒素毒性分子作用机制与脱毒的研究进展

T-2毒素是一种A类单端孢霉烯族毒素,具有高度致毒作用、毒性较难降解等特点,严重威胁人类和动物安全。目前,用于T-2毒素脱毒的方法有物理吸附法、化学试剂中和法、微生物分解法等。但T-2毒素导致的中毒反应的分子机制还尚未明确,可能涉及多个方面,如线粒体损伤、细胞自噬、免疫逃逸、细胞凋亡等。因此,文章主要探讨了T-2毒素毒性作用分子机制以及T-2毒素脱毒的研究进展,为T-2毒素的深入研究提供参考。

ZnO,TiO_2,SiO_2,and Al_2O_3 Nanoparticles-induced Toxic Effects on Human Fetal Lung Fibroblasts

Objective This study aims to investigate and compare the toxic effects of four types of metal oxide （ZnO, TiO2, SiO2, and Al2O3） nanoparticles with similar primary size （-20 nm） on human fetal lung fibroblasts （HFL1） in vitro.Methods The HFL1 cells were exposed to the nanoparticles, and toxic effects were analyzed by using MTT assay, cellular morphology observation and Hoechst 33 258 staining.Results The results show that the four types of metal oxide nanoparticles lead to cellular mitochondrial dysfunction, morphological modifications and apoptosis at the concentration range of 0.25-1.50 mg/mL and the toxic effects are obviously displayed in dose-dependent manner. ZnO is the most toxic nanomaterials followed by TiO2, SiO2, and Al2O3 nanoparticles in a descending order.Conclusion The results highlight the differential cytotoxicity associated with exposure to ZnO, TiO2, SiO2, and Al2O3 nanoparticles, and suggest an extreme attention to safety utilization of these nanomaterials.

5-羟甲基糠醛的急性毒性研究

实验旨在研究5-羟甲基糠醛(5-HMF)对昆明小鼠的急性毒性影响,初步评价产品对昆明小鼠的毒效应特征、靶器官和剂量-反应关系。选取80只SPF级雄性昆明小鼠,随机分为8组,每组10只。适应性饲养一周后,采用8种不同剂量的5-HMF溶液进行口服灌胃。结果表明,昆明小鼠灌胃给药后随剂量增加出现呼吸困难、急促,扎堆、眯眼,被毛竖立而后死亡,随着剂量降低,出现以上现象频率降低。体重方面,与对照组相比,药物对体重无明显影响。利用改良寇式法计算昆明小鼠5-HMF急性毒性LD_(50)为3152.800 mg/kg。存活动物组织病理学检查结果显示:5-HFM毒性靶向器官为肾脏,小叶间静脉旁间质见炎性细胞浸润。根据WHO口服外源毒物分级标准,5-HMF为低毒。

Toxic Effects of Nano-CuO, Micro-CuO and Cu²⁺on <i>Chlorella</i>sp.

The 96 h acute toxic effects of nano-CuO (N-CuO), micro-CuO (M-CuO) and 2+ on Chlorella sp. were investigated in this paper. The results showed that toxicities decreased in an order of Cu2+>N-CuO>M-CuO. The 96 h EC50 of Cu2+ on Chlorella sp. was 1.06 mg /L, and of N-CuO it was 74.61 mg /L, while no pronounced toxicity was observed when the concentration of M-CuO was lower than 160 mg/L. Further experiments were carried out in order to study the toxicity mechanism of nano-CuO on Chlorella sp.. The results of Cu2+ release from N-CuO showed less than 0.2 mg/L Cu2+ were released, so the release of Cu2+ was not responsible for the toxicity. Further experiments showed N-CuO inhibited formation of Chlorophyll A. Content of Chlorophyll A in the control group was 4.75 mg/108 cells, while it declined to 2.89 mg/108 cells for 160 mg/L N-CuO after 96 h, which indicated that N-CuO could inhibit photosynthesis of Chlorella sp.. Moreover, N-CuO condensed with algal cells. It affected the activity of SOD and POD, indicating that N-CuO could cause oxidant stress to Chlorella sp.. These may be the toxicity mechanism.

Histological Assessment and Transcriptome Analysis Provide Insights into the Toxic Effects of Perfluorooctanoic Acid to Juvenile Half Smooth Tongue Sole Cynoglossus semilaevis

Perfluorooctanoic acid(PFOA)is a widespread synthetic persistent organic pollutant that may enrich along the food chain and affect the growth,development,reproduction,and lipid metabolism of aquatic organisms,particularly the benthic organisms.How-ever,the toxic effects of PFOA on the half-smooth tongue sole Cynoglossus semilaevis,a commercial benthic fish in China,have rarely been reported.Because juvenile fish are sensitive to environmental pollutants,in the present study,histological assessment and tran-scriptome sequencing were performed to determine the short-term impact of PFOA on juvenile half-smooth tongue soles.Histologi-cal analysis showed that PFOA exposure caused hepatocyte rupture,intestinal villi breakage,increased goblet cell count,and brain ab-normal.Transcriptome results showed that some interesting signaling pathways,such as glycolysis/gluconeogenesis,PPAR signaling pathway and GABAergic synapse signaling pathway,were enriched after PFOA exposure.In addition,some metabolic,immune and neural genes were differentially expressed,which including ependymin,hbb1-like and gad 1,and they were up-regulated after 14 days of exposure.Transcriptome results also indicated that half-smooth tongue sole might improve energy metabolism in response to PFOA toxicity after 7 days of exposure.These findings provide a basis for studying the ecological effects of PFOA on marine benthic fishes.

Effects of Sub-chronic Intoxication of 1,8-cineole on Blood Biochemical Indexes of Mice

[ Objective] Effects of sub-chronic intoxication of 1,8-cineole on body weights, routine blood indexes and biochemical indexes of mice were investigated. [Method] One hundred and sixty mice with body weights of 15 -17 g were randomly divided into four groups （forty mice per group）. Mice were injected to 1, 8 - cineole with doses of 192.45,64. 15 and 21.38 mg/kg body weight （ test groups） and the water solution of tween-80 with a volume fraction of 0.5% （ control group） respectively. Each mouse was administered orally at the dose of 0.2 mL per 10 g body weight once a day consecutively for 90 d. The body weight, routine blood indexes and serum biochemical indexes of mice were determined on the 30^th d, 60^th d, 90^th d and the 30^th d after stopping the administration of 1,8-cineole. [ Result] The effects of 1, 8-cineole on the body weight, routine blood indexes and serum biochemical indexes of mice with the doses of 64.15 and 21.38 mg/kg body weight had no statistically significant difference compared with the control group （P 〉0.05 ）. 1, 8-cineole with the dose of 192.45 mg/kg body weight exhibited different influences on routine blood indexes and serum biochemical indexes of mice after the oral administration of 1,8-cineole for 60 d and 90 d, and statistically significant differences in many blood biochemical indexes were observed （P 〈 0.05 ）. However, the differences in routine blood indexes and serum biochemical indexes were not statistically significant between the test groups and the control group at the 30＇h d after stopping the administration of 1, 8-cineole （ P 〉 0.05）. [Condusion] 1,8-cineole had sub-chronic oral toxicity to mice. The no observed adverse effect level （NOAEL） of 1,8-cineolc was 64.15 mg/kg body weight and the lowest observed adverse effect level （LOAEL） of 1,8-cineole was 192.45 mg/kg body weight. Effects of 1, 8-cineole on blood biochemical indexes of mice were in short term and reversible.

Protective Effects of Calcium Antagonists on Cadmium-induced Toxicity in Rats

Protective effects of calcium antagonists, chlorpromazine (CPZ) and nimodepine (NI-MO), on cadmium-induced toxicity were investigated. After giving CdCl2 (0. 44mg Cd/kg,ip), CPZ (5mg/kg, ip) or NIMO (8mg/kg, po) were administered every day to Sprague-Dawley (S. D. ) rats for a week. Then, urinary N- acetyl-β-D- glucosaminidase (NAG ), uri -nary cadmium and bloocl cadmium were measured. The accumulation of cadmium in the kid-ney cortex, content of renal calmodulin, hemoglobin and the ultrastructural damage of proxi-mal convoluted tubules of rats were examined three weeks after the last administration. Re-sults indicated that the calcium antagonists partly protected against toxic effects induced bycadmium in different manners. These data provide further evidence for the new hypothesisthat the cross effect of cadmium and calcium in calmodulin regulated systems may be responsi-ble for the mechanism of cadmium intoxication. 'The results suggested that the calcium antag-onists could be a new and promising approach in the therapy of heavy metaLinduced diseases

Toxic Effects of Tetrabromobisphenol A on Thyroid Hormones in SD Rats and the Derived-reference Dose

The present study determined the thyroid hormone interference of tetrabromobisphenol A （TBBPA） in Sprague-Dawley （SD） rats, and the derived-reference dose （RfD） of different endpoint effects on mammals based on experimental results and data collection. Based on repeated exposure toxicity tests on mammals and extensive research, the present study used BMDS240 Software to derive a benchmark dose, and analyzed the accuracy and uncertainty, and similarity with other studies. Test results on triiodothyronine （T3）, thyroxine （T4）, and thyroid stimulating hormone （TSH） demonstrated that all the indicators presented a non-monotonous dose-effect relationship clearly, except TSH in male rats exposed to 0-1000 mg/kg BW per day. Therefore, RfDs were derived from different critical effects. In summary, RfD for mammals in the present study was found to be 0.6 mg/kg per day.

Potential Toxicological and Cardiopulmonary Effects of PM2,5 Exposure and Related Mortality:Findings of Recent Studies Published during 2003-2013

Air pollution has environmental issue owing become a serious to its diverse harmful effects on the physical and biological environment. According to the Environmental Protection Agency （EPA） and the World Health Organization （WHO）, air pollution affects millions of people worldwide. Hundreds of thousands of deaths each year and a range of diseases, particularly among vulnerable groups （i.e., children, the elderly, and people with special medical conditions）, are attributed to air pollution. These effects are not always caused by single pollutant in the air; rather, they are considered consequences of the multi-pollutants to which people are simultaneously exposed.

曲妥珠单抗联合放化疗对HER2阳性乳腺癌患者血清CEA、 CA153、ICAM-1水平的影响

目的探究曲妥珠单抗联合放化疗对人表皮生长因子受体2(HER2)阳性乳腺癌患者癌胚抗原(CEA)、癌相关糖蛋白抗原(CA153)和细胞间黏附因子-1(ICAM-1)的影响。方法按照信封抽签法将110例HER2阳性乳腺癌患者分为观察组(55例,采用放化疗+曲妥珠单抗的治疗方式)与对照组(55例,采用放化疗的治疗方式),比较两组患者的临床疗效、生存时间及质量、血清肿瘤标志物水平和用药安全性。结果对照组患者经治疗后疾病缓解率(43.64%)明显低于观察组(76.36%)(P<0.05);对照组的肿瘤总生存期、无进展生存期和QOL评分等各项数据都明显低于观察组(P<0.05);两组患者治疗后CEA、CA153、ICAM-13均降低,且观察组降低幅度更显著(P<0.05);总不良反应发生率观察组(27.27%)与对照组(23.64%)比较无统计学意义(P>0.05)。结论曲妥珠单抗联合放化疗能够有效改善患者的血清CEA、CA153、ICAM-1水平,提高HER2阳性乳腺癌患者的临床疗效,且不会增加患者机体的不良反应。

Effects of natural-cerebrolysin-containing serum on neurotoxicity and synaptogenesis in amyloid-beta 1-40-induced Alzheimer's disease in vitro models

BACKGROUND： Neuronal loss, synapse mutilation, and increasing malnourished axons are pathologically related to Alzheimer＇s disease. Microtubule-associated protein 2 （MAP2） is of importance for neuronal, axonal, and dendritic generation, extension, and stabilization, as well as for the regulation of synaptic plasticity. OBJECTIVE： To investigate the antagonistic effects of natural-cerebrolysin-containing serum on beta amyloid protein 1-40 （Aβ1-40）-induced neurotoxicity from the standpoints of cell proliferation, synaptogenesis, and cytoskeleton formation （MAP2 expression）. DESIGN, TIME AND SETTING： A paralleled, controlled, neural cell, and molecular biology experiment was performed at the Institute of Integrated Chinese and Western Medicine, Shenzhen Hospital, Southern Medical University between February 2006 and April 2008. MATERIALS： PC12 cells, derived from the rat central nervous system, were purchased from Shanghai Institute of Cell Biology, Chinese Academy of Sciences, China. A β1-40 was provided by Sigma, USA. Natural-cerebrolysin was provided by Shenzhen Institute of Integrated Chinese and Western Medicine, China. The natural-cerebrolysin was predominantly composed of Renshen （Radix Ginseng）, Tianma （Rhizoma Gastrodiae）, and Yixingye （Ginkgo Leaf） in a proportion of 1：2：2. Following conventional water extraction technology, an extract （1：20） was prepared. Each gram of extract equaled 20 grams of crude drug. In a total of 12 adult male New Zealand rabbits, six underwent intragastric administration of natural-cerebrolysin extract for 1 month to prepare natural-cerebrolysin-containing serum, and the remaining six rabbits received intragastric administration of physiological saline to prepare normal blank serum. METHODS： An AIzheimer＇s disease in vitro model was induced in PC12 cells using Aβ1-40. The cells were incubated with varying doses of natural-cerebrolysin-containing serum （2.5%, 5%, and 10%）. Normal blank serum-treated PC12 cells served as a blank control group. MAIN OUTCOME MEASURES： Through the use of inverted phase contrast microscope, cell morphology and neurite growth were observed, neurite length was measured, and the percentage of neurite-positive cells was calculated. Cell proliferation rate was determined by MTT assay, and MAP 2 expression was detected by fluorescent immunocytochemistry. RESULTS： Following Aβ1-40 treatments, some PC12 cells were apoptotic/dying, and only a few short neurites were observed. Following interventions with natural-cerebrolysin-containing serum, the PC12 cells proliferated, there was an increased number of neurites, and neurite length was enhanced. After middle- and high-dose natural-cerebrolysin treatments, the percentage of neurite-positive cells, as well as the average length of neurites, was significantly greater than the normal blank serum-treated PC12 cells （P 〈 0.05 or P 〈 0.01）. Compared with the blank control group, MAP2 expression in the Aβ1-40-treated PC12 cells was significantly inhibited, and the cell proliferation rate was significantly decreased （P 〈 0.01）. Following incubations with natural-cerebrolysin-containing serum, MAP2 expression and cell proliferation rate in the PC12 cells were significantly increased in a dose-dependent manner, compared with treatments with blank control serum （P 〈 0.05 or P 〈 0.01 ）. CONCLUSION： Natural-cerebrolysin exhibited antagonistic effects on neurotoxicity in Aβ1-40 induced Alzheimer＇s disease in vitro models. These effects were likely related to cell proliferation and the upregulation of intracellular MAP2 expression.

R-CDOP方案治疗弥漫大B细胞淋巴瘤的效果及对免疫功能、预后影响

目的探讨R-CDOP方案治疗弥漫大B细胞淋巴瘤的效果及对免疫功能、预后影响。方法选取2017年10月至2020年6月于浙江省台州市中心医院(台州学院附属医院)诊治且随访至2022年7月的52例弥漫大B细胞淋巴瘤患者作为研究对象,按照随机数字表法分为观察组(予以R-CDOP方案治疗)与对照组(予以R-CHOP方案治疗),各26例。比较两组有效率、免疫功能(CD3^(+)、CD4^(+)、CD8^(+))、毒副作用、2年生存率及生存时间。结果观察组客观有效率、完全缓解率高于对照组,差异有统计学意义(P<0.05)。化疗后,两组CD3^(+)、CD4^(+)低于化疗前,且观察组高于对照组;两组CD8^(+)高于化疗前,且观察组低于对照组,差异有统计学意义(P<0.05)。观察组毒副作用总发生率低于对照组,差异有统计学意义(P<0.05)。观察组2年生存率、生存时间高于对照组,差异有统计学意义(P<0.05)。结论R-CDOP方案治疗弥漫大B细胞淋巴瘤效果显著,有利于减轻对免疫功能的影响,且安全性高。

Effect of Certain Toxicants on Gonadotropin-Induced Ovarian Non-Esterified Cholesterol Depletion and Steroidogenic Enzyme Stimulation of the Common Carp Cyprinus carpio in vitro

Isolated ovarian tissues from the common carp, Cyprinus carpio were incubated in vitro to obtain a discrete effect of four common toxicants of industrial origin, namely phenol, sulfide, mercuric chloride and cadmium chloride, on gonadotropin-induced alteration of nonesterified and esterified cholesterol and steroidogenic enzymes, △5-3β-HSD and 17β-HSD activity. Stage II ovarian tissue containing 30-40% mature oocytes were shown to be most responsive to gonadotropins in depleting only nonesterified cholesterol moiety and stimulating the activity of both. Safe doses of above mentioned toxicants when added separately to stage II ovarian tissue with oLH (1 μg/incubation) gonadotropin-induced depletion of nonesterified cholesterol and gonadotropin-induced stimulation of the activity of both enzymes was significantly inhibited. Esterified cholesterol remained almost unaltered. Findings clearly indicate the impairment of gonadotropin induced fish ovarian steroidogenesis by the four toxicants separately.